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SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: 14-53% of coronavirus disease 2019 (COVID-19) patients have elevated alanine aminotransferase(ALT) and aspartate aminotransferase (AST) [1] We present a case of COVID-19 who developed severe metabolic acidosis from acute liver failure CASE PRESENTATION: 53-year-old male with a history of cardiomyopathy (Ejection Fraction [EF] of 15%) was admitted with shortness of breath and tested positive for COVID-19 He was hypoxic (2-3 liters on nasal cannula [NC]) and had a blood pressure (BP) of 100/70 mm of Hg His initial labs were significant for mild elevations in AST and ALT with normal alkaline phosphatase He underwent CT scan of the chest and abdomen, which showed nonspecific lung nodules and thickened gall bladder His liver enzymes began to rise serially reaching an AST of 4,735 and ALT of 1,988 He was treated with convalescent plasma on day 2 of admission Hepatitis panel was negative Ultrasound arterial doppler of the abdomen and HIDA scan ruled out portal vein thrombosis and cholecystitis, respectively He developed tachypnea to 50 breaths/minute and respiratory distress An arterial blood gas showed pH:7 5, pCO2:10, pO2:68, HCO3:10 and a lactate of 16 Initial concerns were for cardiogenic shock (due to low EF) vs sepsis However, BP was stable with good urine output He was transferred to the ICU Repeat echocardiography(TTE) showed an EF of 15-25% He was placed on broad antibiotics and received N-acetylcysteine (NAC) for liver failure Repeat infectious exam and imaging were negative His lactic acidosis improved, and he was downgraded within 48 hours DISCUSSION: Normal BP, evidence of good end organ perfusion, unchanged TTE findings and negative infectious work up ruled out cardiogenic and septic shock Negative hepatitis viral screen, negative imaging tests and absence of hepatotoxic agents ruled out other causes of liver injury NAC administration coincided with clinical improvement, although its role in the recovery process remained unclear Severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] binds to angiotensin-converting enzyme 2 (ACE2) receptor to enter target cells Studies have shown ACE2 receptors to have increased activity in cholangiocytes through which SARS-COV-2 can cause liver injury [2] COVID-19 is known to cause multi-organ failure leading to acidosis However,clinicians must be aware of lactic acidosis from purely COVID-19-induced acute liver failure as seen above CONCLUSIONS: Acute onset lactic acidosis can be indicative of multiple processes which can be challenging to interpret in an urgent setting Respiratory distress in COVID-19 patients is not always due to an acute lung process but may be related to metabolic acidosis induced tachypnea Future studies looking at use of NAC in COVID-19-induced liver failure may be beneficial Reference #1: Zhang, Chao et al “Liver injury in COVID-19: management and challenges ” The lancet Gastroenterology & hepatology vol 5,5 (2020): 428-430 Reference #2: Chai X Hu, L Zhang Y et al Specific ACE2 expression in cholangiocytes may cause liver damage after 2019-nCoV infection bioRxiv 2020;(published online Feb 4 ) DISCLOSURES: No relevant relationships by Lee-Gardie Jean, source=Web Response No relevant relationships by Nicole Rapista, source=Web Response No relevant relationships by Sauradeep Sarkar, source=Web Response
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